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Results for “Reperfusion”

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At least 145 records · Page 8Linked to original sources

PubMed1998

Optimizing the oxygen balance during initial reperfusion with 2,3-butanedione monoxime attenuates cardiac reperfusion injury.

The effect of 20 mmol/L butanedione monoxime on myocardial ischemia/reperfusion damage was studied in isolated guinea pig hearts. Three groups of hearts (n = 8) were perfused in the Langendorff mode and cardioplegic arrest was induced with St. Thomas Hospital II solution (STS) at 37 degrees C for 50 min. Myocardial oxygen demand, recovery of myocardial function, and creatine kinase release during 30 min of reperfusion were monitored. Preservation of myocardial ultrastructure was determined by electron microscopy. Control (C) hearts underwent cardioplegic arrest and reperfusion without treatment. BDM was added during cardioplegic arrest in BDMSTS hearts, or to the initial (20 min) reperfusate in BDMREP hearts. BDM during initial reperfusion markedly reduced O2 demand and prevented creatine kinase release from cardiac myocytes, resulting in improved recovery of myocardial function and attenuation of myocardial ultrastructural damage after washout of the drug. In contrast, addition of BDM to the cardioplegic solution provided no protection from ischemic or reperfusion injury.

Animals↗

PubMed2004

Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion.

OBJECTIVE: We previously showed that brief intermittent ischemia applied during the onset of reperfusion (i.e., postconditioning) is cardioprotective in a canine model of ischemia-reperfusion. This study tested the hypothesis that the early minutes of reperfusion (R) during which postconditioning (Post-con) is applied are critical to its cardioprotection. METHODS: In anesthetized open-chest rats, the left coronary artery (LCA) was occluded for 30 min and reperfused for 3 h. All rats were randomly divided into six groups: Control (n=8): no intervention at R; Ischemic preconditioning (IPC) (n=8): the LCA was occluded for 5 min followed by 10 min of R before the index occlusion; Post-con 1 (n=8): after LCA occlusion, three cycles of 10 s R followed by 10 s LCA re-occlusion were applied during the first minute of R; Post-con 2 (n=8): Six cycles of 10 s R and 10 s re-occlusion were applied during the first 2 min of R; Delayed Post-con (n=8): the ligature was loosened for full reflow for the first minute of R, after which the three-cycle Post-con algorithm was applied; Sham (n=6): the surgical procedure was identical to other groups, but the LCA ligature was not ligated. RESULTS: Infarct size (TTC staining) was 23% smaller in Post-con 1 (40+/-2%*) than in Control (52+/-3%), confirmed by plasma creatine kinase activity (18+/-2* vs. 46+/-6 IU/g protein). There was no further reduction in infarct size with 6 cycles of Post-con (40+/-2.9%, p>0.05 vs. Post-con 1). Meanwhile, infarct size reduction was significantly greater in the IPC group (17+/-3%) than in Post-con1 (p<0.01). The plasma lipid peroxidation product malondialdehyde (MDA, microM/ml) was less after R in IPC and Post-con 1 (0.8+/-0.07* and 0.8+/-0.06*) vs. Control (1.21+/-0.08), consistent with a visual decrease in superoxide anion generation (dihydroethidium staining) in the AAR myocardium after 3 h of reperfusion. Neutrophil accumulation (myeloperoxidase activity, MPO, U/100 g tissue) in the AAR was less in IPC (1.4+/-0.3*) and Post-con 1 (2.5+/-0.3*) vs. Control (5.5+/-0.6). The reductions in infarct size, creatine kinase, MDA and DHE staining were lost with delayed Post-con, while MPO activity remained lower than in Control (3.2+/-0.4*). CONCLUSIONS: (1) Post-con at onset of R reduces myocardial injury; (2) cardioprotection may be mediated, in part, by inhibiting oxidant generation and oxidant mediated injury; (3) the first minute of R in the rat model is critical to cardioprotection by Post-con; and (4) cardioprotection by Post-con may be independent of neutrophil accumulation in AAR. *p<0.05 Post-con vs. Control.

Animals↗

PubMed2000

A controlled trial of substrate-enhanced, warm reperfusion ("hot shot") versus simple reperfusion.

BACKGROUND: Modified reperfusion after aortic cross-clamping is claimed to reduce myocardial injury, thus improving postoperative myocardial performance. METHODS: We measured perioperative release of creatine kinase-MB and troponin-T in 40 patients undergoing valve replacement (combined with coronary grafts in 12 cases) to determine whether infusion of a modified reperfusate before cross-clamp removal reduced myocardial injury. Patients were randomly allocated to one of two groups with minimization for age, surgeon, operation, and ventricular function. The control group received unmodified reperfusion, while the study group received a normothermic reperfusate, enhanced with glutamate and aspartate, for 5 minutes before removal of the cross-clamp. Serial determinations of troponin-T, creatine kinase-MB isoforms, and total creatine kinase-MB activity were made up to 5 days postoperatively. Requirements for inotropic support and evidence of myocardial infarction were documented. RESULTS: Creatine kinase-MB activity, creatine kinase-MB isoforms, and troponin-T were not significantly different between the two groups. There were no differences in the incidence of postoperative myocardial infarction or in inotrope requirement. CONCLUSIONS: Our study did not demonstrate any advantage in using modified reperfusion in this group of patients.

Adult↗

PubMed2003

Deep hypothermic circulatory arrest and global reperfusion injury: avoidance by making a pump prime reperfusate--a new concept.

OBJECTIVE: We sought to determine whether damage after deep hypothermic circulatory arrest can be diminished by changing pump prime components when reinstituting cardiopulmonary bypass. METHODS: Fifteen piglets (2-3 months old) were cooled to 19 degrees C by using the alpha-stat pH strategy. Five were cooled and rewarmed without ischemia (control animals), and the other 10 piglets underwent 90 minutes of deep hypothermic circulatory arrest. Of these, 5 were rewarmed and reperfused without altering the cardiopulmonary bypass circuit blood prime. In the other 5 animals, the bypass blood prime was modified (leukocyte depleted, hypocalcemic, hypermagnesemic, pH-stat, normoxic, mannitol, and an Na(+)/H(+) exchange inhibitor) during circulatory arrest before starting warm reperfusion. Oxidant injury was assessed on the basis of conjugated dienes, vascular changes on the basis of endothelin levels, myocardial function on the basis of cardiac output and dopamine need, lung injury on the basis of pulmonary vascular resistance and oxygenation, and cellular damage on the basis of release of creatine kinase and aspartate aminotransferase. Neurologic assessment (score 0, normal; score 500, brain death) was done 6 hours after discontinuing cardiopulmonary bypass. RESULTS: Compared with animals undergoing cardiopulmonary bypass without ischemia (control animals), deep hypothermic circulatory arrest without modification of the reperfusate produced an oxidant injury (conjugated dienes increased 0.78 vs 1.71 absorbance (Abs) 240 nmol/L per 0.5 mL, P <.001 vs control animals), depressed cardiac output (6.0 vs 4.0 L/min, P <.05 vs control subjects), prolonged dopamine need (P <.001 vs control subjects), elevated pulmonary vascular resistance (74% vs 197%, P <.05 vs control subjects), reduced oxygenation (P <.01 vs control subjects), increased neurologic injury (56 vs 244, P <.001 vs control subjects), and increased release of creatine kinase (2695 vs 6974 U/L, P <.05 vs control subjects), aspartate aminotransferase (144 vs 229 U/L), and endothelin (1.02 vs 2.56 pg/mL, P <.001 vs control subjects). Conversely, the oxidant injury was markedly limited (conjugated dienes of 0.85 +/- 0.09 Abs 240 nmol/L per 0.5 mL, P <.001 vs unmodified pump prime) with modification of cardiopulmonary bypass prime, resulting in increased cardiac output (5.1 +/- 0.8 L/min), minimal dopamine need (P <.001 vs unmodified pump prime), no increase in pulmonary vascular resistance (44% +/- 31%, P <.01 vs unmodified pump prime) or endothelin levels (0.64 +/- 0.15 pg/mL, P <.001 vs unmodified pump prime), complete recovery of oxygenation (P <.01 vs unmodified pump prime), reduced neurologic damage (144 +/- 33, P <.05 vs unmodified pump prime), and lower release of aspartate aminotransferase (124 +/- 23 U/L, P <.05 vs unmodified pump prime) and creatine kinase (3366 +/- 918, P <.05 vs unmodified pump prime). CONCLUSIONS: A global reperfusion injury after deep hypothermic circulatory arrest was identified and changed. The injury is mediated by oxygen-derived free radicals, resulting in organ and endothelial dysfunction. Modification of global organ and endothelial damage is achieved by modifying the blood prime in the cardiopulmonary bypass circuit to deliver a controlled global reperfusate when reinstituting bypass.

Animals↗

PubMed1995

Infarct salvage with liposomal prostaglandin E1 administered by intravenous bolus immediately before reperfusion in a canine infarction-reperfusion model.

BACKGROUND: Prostaglandin E1 (PGE1) inhibits leukocyte and platelet function and reduces infarct size during left atrial infusion. Intravenous liposomal PGE1 (TLC C-53) accelerates thrombolysis and prevents reocclusion in canine coronary thrombosis. We tested the hypothesis that intravenous TLC C-53 would attenuate reperfusion injury in a canine infarction-reperfusion model. METHODS AND RESULTS: Twenty-one open-chest dogs were randomized to receive a 10-minute intravenous infusion of either liposome diluent (placebo), free PGE1 (2 micrograms/kg), or TLC C-53 (2 micrograms/kg PGE1) after 2 hours of left anterior descending (LAD) occlusion just before reperfusion. Hemodynamic assessment, regional myocardial blood flow determination with radioactive microspheres, myocardial leukocyte infiltration by myeloperoxidase assay, and estimation of infarct size using triphenyl tetrazolium chloride staining were performed. Regional fractional shortening was measured with sonomicrometer crystals implanted in the midmyocardium. Infarct size as a percentage of the risk region was significantly reduced (P < .05) with TLC C-53 (37.9 +/- 17.4%) compared with PGE1 (56.7 +/- 13.9%) or placebo (58.0 +/- 9.9%) infusion. Infarct salvage with TLC C-53 was independent of collateral blood flow by ANCOVA. There was a dramatic reduction in myeloperoxidase activity in the infarct, risk, and border regions of dogs treated with TLC C-53 compared with placebo. Enzyme activity was also significantly reduced (P < .05) in the infarct zone with TLC C-53 (0.11 +/- 0.1 U/100 mg) treatment compared with PGE1 (0.38 +/- 0.3 U/100 mg). No significant differences in regional myocardial blood flow or myocardial function among treatment groups were identified, although there was a trend toward improved function in the TLC C-53 dogs. CONCLUSIONS: Bolus intravenous administration of TLC C-53 immediately before reperfusion results in reduced leukocyte infiltration and substantial infarct salvage. TLC C-53 mah be useful in limiting reperfusion injury during treatment of acute myocardial infarction.

Alprostadil↗

PubMed1989

"Reperfusion injury" by oxygen-derived free radicals? Effect of superoxide dismutase plus catalase, given at the time of reperfusion, on myocardial infarct size, contractile function, coronary microvasculature, and regional myocardial blood flow.

Do oxygen-derived free radicals, generated at the time of reperfusion, lethally injure viable, previously ischemic myocardium, damage vascular endothelium, and impair recovery of postischemic contractile function? To address these issues, 23 anesthetized open-chest dogs underwent 2 hours of left anterior descending coronary artery occlusion followed by 4 hours of reperfusion. Immediately prior to reflow, each dog was randomized to receive either the free radical scavenging agents superoxide dismutase (SOD) + catalase, or saline alone. SOD + catalase had no significant beneficial effect on infarct size measured by triphenyltetrazolium staining: area of necrosis averaged 38.5 +/- 6.1% vs. 46.3 +/- 6.2% of the area at risk in treated compared with control animals respectively (p = NS). Furthermore, infusion of SOD + catalase did not alter contractile function of the viable subepicardium: mean segment shortening (measured using sonomicrometry) at 4 hours postreperfusion was -23 +/- 5% of baseline, preocclusion values in controls dogs and -24 +/- 9% of preocclusion values in animals that received the scavenging agents. However, SOD + catalase treatment preserved the endocardial microvasculature (assessed by semiquantitative electron microscopic analysis) and enhanced regional myocardial blood flow after reperfusion. Specifically, mean score for microvascular injury was 0.41 +/- 0.14 vs. 0.10 +/- 0.08 (p less than 0.05) in control compared with SOD + catalase treated groups, and blood flow averaged 0.56 +/- 0.11 vs. 1.27 +/- 0.33 ml/min/g tissue (p less than 0.05), respectively, in the previously ischemic endocardium at 2 hours postreflow. Thus, SOD + catalase given at the time of reperfusion had no acute beneficial effect on either the extent of myocyte necrosis or postischemic contractile function in this canine model. SOD + catalase did, however, attenuate both endocardial vascular injury and the "low reflow" phenomenon. These data suggest that microvascular injury and low reflow following prolonged (2 hour) but transient coronary occlusion may be mediated by oxygen-derived free radicals generated at the time of reperfusion.

Animals↗

PubMed1990

Reperfusion and reperfusion injury in acute myocardial infarction.

Recognition of the clinical markers of reperfusion and comprehension of the effects of reperfusion injury in acute myocardial infarction provide a unique challenge for today's critical care nurse. In this article we will explore the processes of reperfusion injury. A review of relevant literature and presentation of a clinical case study and care plan will enable the critical care nurse to construct a larger knowledge base and assist in the nursing management of patients with acute myocardial infarction. Evaluation and treatment of reperfusion and reperfusion injury remains under investigation, but through the skills of assessment, planning, and intervention the critical care nurse can coordinate prompt and appropriate care to the patient with an acute myocardial infarction.

Critical Care↗

PubMed1991

Ischemia-reperfusion arrhythmias and lipids: effect of human high- and low-density lipoproteins on reperfusion arrhythmias.

The effect of high- and low-density lipoproteins separated from human serum on the postischemic reperfusion arrhythmias was investigated. The hearts were perfused by working heart mode with Krebs Henseleit bicarbonate buffer containing arachidonic acid (1 microgram/ml) for 5 minutes. Whole heart ischemia was induced by the use of a one-way ball valve, and hearts were perfused for 15 minutes followed by 20 minutes of reperfusion. Physiologic concentrations of high- and low-density lipoproteins were constantly infused through the atrial route during ischemic perfusion. Coronary effluent was collected via pulmonary artery cannulation for subsequent radioimmunoassay of thromboxane B2 and 6-keto-prostaglandin F1 alpha, the major stable metabolites of thromboxane A2 and prostacyclin, respectively. The incidence of ventricular arrhythmias during reperfusion was 6/6 (100%), 1/6 (17%), and 6/6 (100%) in control, high-density lipoprotein and low-density lipoprotein infusion groups, respectively. There was no significant difference in coronary flow among the three groups throughout the perfusion. Both thromboxane B2 and 6-keto-prostaglandin F1 alpha increased significantly during ischemia compared with preischemic values in all groups of hearts. However, the ratio of these two parameters varied in control and low-density lipoprotein infusion groups during ischemia, while there was no significant change in the high-density lipoprotein infusion group. These results provide the possibility that arachidonate metabolites may be involved in the regulation of ischemia-reperfusion arrhythmias and that high-density lipoprotein that was infused during ischemia markedly inhibits the incidence of ischemia-reperfusion-induced ventricular arrhythmias, due in part at least, to stabilizing the arachidonate metabolites during ischemic perfusion.

Animals↗

PubMed1995

R56865 is antifibrillatory in reperfused ischemic guinea-pig hearts, even when given only during reperfusion.

R56865 was previously characterized as an inhibitor of Na and Ca overload that has beneficial effects during ischemia and reperfusion. An isolated guinea-pig heart preparation was subjected to 60 minutes of ischemia and 60 minutes of reperfusion. R56865 was given before ischemia and with the onset of reperfusion, applying different dosing schedules, including an initial loading dose. R56865 below 0.1 mumol/l had no cardiodepressant effects in normoxic hearts and at 0.1 mumol/l reduced left ventricular pressure marginally. The onset of ischemic contracture was delayed only at this concentration. R56865 given before ischemia potently inhibits delayed sustained fibrillation occurring during reperfusion in the concentration range between 0.01 mumol/l and 0.1 mumol/l. Analysis of cellular Na+, K+, and Ca2+ concentrations revealed that R56865 substantially improves the ionic homeostasis of myocardial cells. Most importantly, the compound also reduced the incidence of delayed sustained fibrillation when given at the onset of reperfusion. R56865 was most effective when fast equilibration of drug with tissue was achieved by giving an initial loading dose. In particular, the cellular Na+ and Ca2+ contents were improved using this dosing scheme. The results are compatible with the classification of R56865 as an inhibitor of Na+ and Ca2+ overload.

Animals↗

PubMed2002

Mannitol dose-dependently attenuates lung reperfusion injury following liver ischemia reperfusion: a dose-response study in an isolated perfused double-organ model.

We had previously studied different modes of prevention of liver ischemia-reperfusion (IR)-induced remote organ reperfusion injury, a challenge that remains partly unmet. We have now studied the capability of mannitol at different doses in abrogating liver IR-induced lung reperfusion injury in an isolated double-organ model. Rat livers ( n = 8/group) were perfused with Krebs-Henseleit solution (control) or made globally ischemic (IR) for 2 h, after which they were paired with normal lungs and "reperfused" together for 15 min. The lungs were then perfused alone with the accumulated Krebs for an additional 45 min. Another 4 control and 4 IR pairs were reperfused with Krebs containing mannitol at.22 mmol,.55 mmol,.77 mmol, or 1.1 mmol. Mannitol.22 mmol and 1.1 mmol failed to attenuate IR-lung injury as indicated by 50-95% increases in inspiratory and perfusion pressures and compliance reduction, a 70% increase in weight gain, and a 2-50-fold increase in bronchoalveolar lavage volume and content. Mannitol.55 mmol prevented all these abnormalities, and.77 mmol attenuated only changes in ventilatory parameters. The latter two treatments were also associated with a 50% reduction in xanthine oxidase activity and a 35-45% increase in the reduced glutathione tissue content compared with the nontreated IR-paired lungs. It is concluded that mannitol in a narrow therapeutic dose range can reduce oxidalive stress-induced lung damage that is related to liver IR.

Animals↗

PubMed1998

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion.

OBJECTIVES: We sought to examine the hypothesis that rapid resolution of ST-segment elevation in acute myocardial infarction (AMI) patients with early peak creatine kinase (CK) after thrombolytic therapy differentiates among patients with early recanalization between those with and those without adequate tissue (myocardial) reperfusion. BACKGROUND: Early recanalization of the epicardial infarct-related artery (IRA) during AMI does not ensure adequate reperfusion on the myocardial level. While early peak CK after thrombolysis results from early and abrupt restoration of the coronary flow to the infarcted area, rapid ST-segment resolution, which is another clinical marker of successful reperfusion, reflects changes of the myocardial tissue itself. METHODS: We compared the clinical and the angiographic results of 162 AMI patients with early peak CK (< or =12 h) after thrombolytic therapy with (group A) and without (group B) concomitant rapid resolution of ST-segment elevation. RESULTS: Patients in groups A and B had similar patency rates of the IRA on angiography (anterior infarction: 93% vs. 93%; inferior infarction: 89% vs. 77%). Nevertheless, group A versus B patients had lower peak CK (anterior infarction: 1,083+/-585 IU/ml vs. 1,950+/-1,216, p < 0.01; and inferior infarction: 940+/-750 IU/ml vs. 1,350+/-820, p=0.18) and better left ventricular ejection fraction (anterior infarction: 49+/-8, vs. 44+/-8, p < 0.01; inferior infarction: 56+/-12 vs. 51+/-10, p=0.1). In a 2-year follow-up, group A as compared with group B patients had a lower rate of congestive heart failure (1% vs. 13%, p < 0.01) and mortality (2% vs. 13%, p < 0.01). CONCLUSIONS: Among patients in whom reperfusion appears to have taken place using an early peak CK as a marker, the coexistence of rapid resolution of ST-segment elevation further differentiates among patients with an opened culprit artery between the ones with and without adequate myocardial reperfusion.

Angioplasty, Balloon, Coronary↗

PubMed2003

Pharmacologic pre-conditioning and controlled reperfusion prevent ischemia-reperfusion injury after 30 minutes of hypoxia/ischemia in porcine hearts.

BACKGROUND: Hearts from non-heart-beating organ donors are not transplanted because of risk of ischemia-reperfusion injury. We tested whether pharmacologic pre-conditioning with adenosine and the Na(+)/H(+) exchanger inhibitor, cariporide, combined with controlled reperfusion, would prevent injury in porcine hearts that had sustained 30 minutes of hypoxia/ischemia in closed-chest animals. METHODS: Hearts from Yorkshire pigs (100 kg) were studied in 3 groups. Group 1 (control) hearts were surgically removed while beating. Group 2 hearts were harvested from animals made hypoxic by discontinuing mechanical ventilation for 30 minutes. Group 3 hearts were hypoxic as in Group 2, but these animals received adenosine (40 mg) and cariporide (400 mg) 10 minutes before stopping ventilation. Cardiac function in all groups was assessed ex vivo in a working heart apparatus in which pressure and flow measurements were made over 3 hours. Controlled reperfusion in Group 3 hearts used leukocyte-depleted blood perfusate containing free radical scavengers. Myocardial injury was assessed on the basis of perfusate creatine phosphokinase activity and histopathologically determined injury score. RESULTS: Groups 1 and 3 hearts could be resuscitated to perform work equivalently during the entire reperfusion period and showed positive responses to increases in pre-load and norepinephrine. Group 2 hearts could not perform work. After 3 hours, Group 2 hearts showed significantly higher creatine phosphokinase and histopathologic injury scores compared to with Groups 1 and 3, which were not significantly different from each other. CONCLUSIONS: Pharmacologic pre-conditioning and controlled reperfusion effectively protect non-beating porcine hearts from injury after 30 minutes of hypoxia/ischemia in situ.

Adenosine↗

PubMed1992

Coronary reperfusion rates in acute myocardial infarction patients after thrombolytic treatment with anistreplase: correlation with the delay from onset of symptoms to treatment: a review of 424 case records of patients admitted to coronary reperfusion studies with anistreplase.

The individual data for 424 acute myocardial infarction patients from 15 reperfusion studies conducted with anistreplase were reviewed to assess the correlation between the delay onset of symptoms to treatment and reperfusion of the coronary artery. The patients had a mean age of 56 years and 85.4% were male. All patients had a baseline angiogram showing an occluded coronary artery. Anistreplase was given in doses ranging from 3.75 to 35 IU (60% of patients received 30 IU). The mean delay between onset of symptoms to treatment was 3 h 29 min and reperfusion was observed in a total of 61.1% of patients. There was a highly significant correlation between reperfusion and the delay from onset of symptoms to treatment (p less than 0.001). A multivariate logistic regression was performed adjusting for age, sex, location of infarct, dose, and concomitant treatment. The only remaining statistically significant prediction factor for reperfusion was the delay between onset of symptoms to treatment (p less than 0.001). In conclusion, the ability of anistreplase to cause the lysis of coronary thrombi appears to be increasingly important as the delay from onset of symptoms to treatment is decreased. This may contribute to the lower mortality rate observed with early fibrinolytic treatment.

Acute Disease↗

PubMed1992

Effect of cloricromene during ischemia and reperfusion of rabbit hindlimb: evidence for an involvement of leukocytes in reperfusion-mediated tissue and vascular injury.

The involvement of polymorphonuclear leukocytes (PMN) in reperfusion-mediated vascular injury was studied in a model of ischemia and reperfusion in rabbit hindlimb. Ischemia was induced by 4-h occlusion of the left iliac artery followed by 4-h reperfusion. Plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activities, hindlimb vascular resistance (HVR), and myeloperoxidase (MPO) activity in the postischemic extensor digitorum longus (EDL) muscle were measured to evaluate the extent of vascular and skeletal muscle injury. In addition, the ischemia/reperfusion-induced injury of the hindlimb vasculature was evaluated by electron microscopy. Ischemia and reperfusion (n = 10) was associated with an increase in CK (6,380 +/- 1,346 U/L, p < 0.05) and LDH (552 +/- 76 U/L, p < 0.05) activities which were significantly greater than those observed in sham-operated control animals (CK 1,651 +/- 207 U/L, LDH 246 +/- 14 U/L; n = 6). HVR in sham-operated animals decreased by 20 +/- 3%, but increased in the ischaemic group by 56 +/- 16% (p < 0.05). MPO activity of EDL muscle increased from 7.3 +/- 3.9 U per muscle (sham) to 28.0 +/- 5.9 U per muscle (p < 0.05) after ischemia and reperfusion. Morphologic analysis did not show any alteration in the microvascular bed of the hindlimb. Moreover, 1 mg/kg/h intravenous (i.v.) cloricromene, an antithrombotic drug that inhibits superoxide anion production as well as PMN adhesion to endothelium, reduced the increase in plasma CK and LDH and the increase in MPO and HVR observed in animals subjected to hindlimb ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Early administration of fluvastatin, but not at the onset of ischemia or reperfusion, attenuates myocardial ischemia-reperfusion injury through the nitric oxide pathway rather than its antioxidant property.

BACKGROUND: Three-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are known to attenuate myocardial ischemia-reperfusion (IR) injury. Fluvastatin (FV) has a potent free radical scavenging action, but it is unclear whether the timing of FV administration could affect its cardioprotective effect or if the antioxidant property of FV might attenuate IR injury. METHODS AND RESULTS: IR was induced in rats by left coronary artery occlusion for 30 min followed by 24-h reperfusion. The rats were divided into 4 groups: oral FV group (10 mg/kg per day for 2 weeks before ischemia); iv, FV group (10 mg/kg) before ischemia; iv, FV group (10 mg/kg) before reperfusion; and control group. Oxidative stress was evaluated by myocardial 8-hydroxydeoxyguanosine (8-OHdG) content. The area at risk did not different among the 4 groups. Pretreatment with FV for 2 weeks significantly reduced the infarct size by 28% as compared with the control group, but FV administered just before ischemia or reperfusion did not. Myocardial 8-OHdG content was not affected by FV. The infarct-sparing effect of FV was completely abolished by N(omega)-nitro-l-arginine methyl ester or wortmannin. CONCLUSIONS: The present results indicate that pretreatment with FV, but not just before ischemia or reperfusion, attenuates IR injury primarily through the nitric oxide pathway, not through its antioxidant property.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1995

Effects of early coronary reperfusion on the time course of signal-averaged electrocardiogram after myocardial infarction and its relation to late arrhythmic events, effects of early coronary reperfusion on signal-averaged ECGs.

The effect of early reperfusion on the time course of signal-averaged ECG was examined in 90 patients with myocardial infarction. Abnormal signal-averaged ECG disappeared more frequently (p < 0.05) and earlier in cases with early reperfusion than in those without. Serious arrhythmic events in the late phase (> 7 days) occurred in patients with abnormal signal-averaged ECG, but not in cases with early reperfusion. These results indicate that dynamic changes in tissue structure and the physiological state of viable muscles after early reperfusion produce different time courses for signal-averaged ECG. The risk of arrhythmic events among patients with abnormal signal-averaged ECG seems to be lower in cases with early reperfusion than in those without.

Aged↗

PubMed1992

Perfluorochemical reperfusion limits myocardial reperfusion injury after prolonged hypothermic global ischemia.

The ability of an oxygenated perfluorochemical (Fluosol) to limit myocardial reperfusion injury following global hypothermic ischemic insult was investigated. Neonatal piglet hearts were arrested with cold crystalloid cardioplegia and stored for 12 hours in 2 degrees C saline. Reperfusion was carried out using an isolated, blood-perfused, working heart preparation. Hearts were initially reperfused (10 minutes) with either whole blood (WB, n = 6), unmodified perfluorochemical (PFC, n = 8), or aspartate/glutamate-enriched perfluorochemical cardioplegia (PFC+, n = 6), prior to institution of whole blood perfusion, functional evaluation and left ventricular biopsy. A control group (C, n = 7) was evaluated without an intervening period of ischemia. At a left ventricular diastolic pressure of 9 mm Hg WB hearts developed a left-ventricular stroke work index (SWI) of 3.8 +/- 2.3 x 10(3) erg/g (mean +/- standard error of the mean). Under similar conditions, PFC-reperfused hearts achieved a SWI of 14.6 +/- 1.3 x 10(3), significantly greater than that of WB (p less than 0.001). SWI for PFC+ hearts was 19.8 +/- 1.6 x 10(3), significantly increased over that of PFC (p less than 0.01), and not different from values obtained for C (19.2 +/- 0.8 x 10(3)). In addition, PFC-reperfused hearts demonstrated superior maintenance (p less than 0.05) of ATP (2.08 +/- 0.16 umole/g), compared to WB (1.50 +/- 0.19), while preservation of ATP in PFC+ hearts (2.99 +/- 0.12), was significantly increased over that of PFC (p less than 0.001), and not significantly different from that for C (2.68 +/- 0.17).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1998

[Optimal reperfusion therapy in acute myocardial infarction: time to reperfusion and recanalization rate].

Rapid and complete reperfusion is important for the reduction of infarct size and mortality in acute myocardial infarction. The optimum reperfusion therapy with regard to the recanalization rate and the time elapsing between onset and complete reperfusion was evaluated. One hundred fifty-four patients with total occlusion of the infarct-related artery within 6 hours of the onset were classified into four therapy groups: PTCA group (n = 58) undergoing primary percutaneous transluminal coronary angioplasty (PTCA), t-PA-IC group (n = 44) receiving tissue plasminogen activator (t-PA) intracoronary infusion, t-PA-IV group (n = 14) receiving intravenous t-PA infusion, and mt-PA-IV group (n = 38) receiving intravenous mutant t-PA infusion. Although the recanalization rate was high in the PTCA group, there were no differences between the four groups as a supplement to immediate or rescue PTCA. The time elapsing between initiation of thrombolysis and complete reperfusion was shorter in the mt-PA-IV group than in the t-PA-IV group. Assuming the time from hospital arrival to initiation of intravenous thrombolysis was 20 min, the recanalization rate at 60 min after arrival in hospital was higher in the mt-PA-IV group than the PTCA and t-PA-IC groups. Although additional coronary angiography and PTCA may be required to improve the low recanalization rate compared with primary PTCA, intravenous infusion of mutant t-PA was the most promising therapy to achieve early reperfusion.

Aged↗